February 25, 2004
Dear Karl Loren,
I came across your site while looking up the VAP test for a lecture and became
intrigued by your premise. While I I've read less than .5% of your 15,000 web
pages, I have read a substantial number of the ones relating to cholesterol.
You paint a fascinating conspiracy theory.
While interesting, they do not take you where you need to go -- the story on plaque does.
All diet related -- I have the total solution on several hundred pages.
What a threat! Well, I invite your many messages, and hopefully we can both learn.
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therapy is valid -- death of bypass surgery and a finally an honest
procedure. Plaque exists where Karl says it is, not where your doctor
says it is located.
The truth about the risk to your heart from high cholesterol levels -- October 2, 2002. This is the nail in the coffin of the cardiologist who makes false claims to put you on dangerous drugs. The ultimate primer on free radicals -- the cause of all heart disease and cancer -- October 2, 2002. Karl's lucid and thorough description of the source of disease that cannot be addressed by either drugs or surgery. Not Subscribed to the Wednesday Letter yet? You can subscribe by filling in your name and email address in the boxes below, and clicking on Subscribe.
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References From The Previous Newsletter -- September 25, 2002 Do YOU need oral chelation? What results can you expect? When? How long should you take it? September 28, 2002. I am the world's expert on oral chelation. We sell more of this product than all others combined. If you haven't read about it? Click now! Does oral chelation prevent or even cure cancer? September 28, 2002. What did Linus Pauling have to say on this and why is it dangerous to ask someone this question? What is ORAL CHELATION anyway? September 28, 2002. If you haven't read a simple basic explanation, this is it. What are the differences between EDTA, and the two other substances, Cysteine and N Acetyl Cysteine in the formulas? September 28, 2002. This is more basic stuff -- good to refresh yourself on if you have already read it, or good to send to someone new. |
Karl Loren
Webmaster
Thanks for giving me a good starting point for investigating cholesterol.
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Best regards,
Patrick Heyman, PhD, ARNP-BC
Assistant Professor
School of Nursing
Palm Beach Atlantic University
901 South Flagler Dr.
West Palm Beach, FL 33416
(561) 803-2829 Office
(561) 803-2828 Fax
Received 25 February 2004
Dear Patrick,
I sent you another e-mail recently about the cholesterol hypothesis and then came across this page. The hypothesis you have is fascinating. It would certainly explain a few things. I'd like to clarify four things that you expound upon.
It would seem easiest to me to put aside these paragraphs you wrote before reading my article on plaque.
I would say, only generally, that false information of the "best" kind is made up of words that have, each of them, a "usual" definition, but in the context in which they are used there is often none of those standard possible definitions that will fit. I've written, majorly, about this when I re-defined a word, "psychobabble," just that way.
That article is here:
http://www.chelationtherapyonline.com/anatomy/p9.htm
This is heavy reading, but it explains my general concept of many of the concepts you develop in those four paragraphs.
In contrast, I hope, my writing uses words which, each, have a usual definition, and the words are used in those senses.
When you try to make sense out of psychobabble it is maddening! I'll leave that go for now.
1. The current hypothesis of "plaque" formation is dependent on endothelial dysfunction. It says that lipoproteins regularly infiltrate the endothelium and then exit back into the artery lumen without causing any damage. Then "something" happens to the endothelial lining and lipoproteins are trapped beneath the lipoprotein, which then become oxidized, etc. The end result is a "plaque" that has a layer of endothelial cells lining it. Your hypothesis takes this idea one step further by having the lesion BE the endothelial cell, while also exonerating the lipoprotein.
2. Plaques or lesions (or inflamed cells) can grow either into the artery lumen--which are the traditional plaques, or they can grow into the tunica media, or middle layer of the cell. This is called arterial remodeling and was first published from the Korean War autopsies. Most acute heart attacks are currently attributed to ruptured lesions which cause a thrombotic event. It is thought that remodeled lesions are more fragile and likely to rupture than traditional lesions. It is also thought that the more calcified a lesion, the more stabile it is. Thus stripping calcium would actually be detrimental. Your hypothesis coupled with your explanation of chelation's mechanism better explains the benefit than traditional theory. This theory also explains why tissue ACE inhibitors seem to have such a beneficial effect.
3. I would add that radiopaque angiography also relies on comparing adjacent segments to determine "disease". This coupled with arterial remodeling above explain how someone can have a "clean cath" and then have a heart attack a month later. And you're absolutely right about caths causing heart attacks.
4. You have a small error on the page. In describing an angiogram, you say that a tube is inserted into a vein, when it should be an artery.
I find this intriguing. I've always thought this procedure went in through a vein. As I checked on the web I found dozens of references to entering a "vessel" without saying which one. I also found references to "intravenous" which implies a vein.
Finally I found the following:
Although each hospital may have specific protocols in place, generally, an arteriogram procedure follows this process:
- The patient is positioned on the x-ray table.
- An intravenous line is inserted into a vein in the patient's arm.
- The patient is connected to an EKG monitor that records the electrical activity of the heart and monitors the heart during the procedure using small, adhesive, electrode patches.
- A small incision is made in the arm or groin, into which a small catheter is inserted.
- The catheter is threaded into the desired vein or artery. (Source)
That seems to indicate that the catheter can be put into a vein or artery. I would expect that you have the more correct data.
It interesting. I was in the midst of writing this e-mail when I received your response from my earlier e-mail. I'm slowly getting where I need to go.
Also in response to your response:
1. You're right, you don't call it a conspiracy theory which has a negative connotation.
2. You're absolutely right about man being mortal. Unfortunately, modern medicine has stripped death of its dignity.
4. Metbolic syndrome is the combination of central obesity, high triglycerides, low HDL, raised blood pressure, insulin resistance, pro-inflammatory state (high HS CRP), and prothrombotic state.
I think you might say the guy is fat because his diet is terrible, probably much too high in carbohydrates?? I have more than 3000 pages about "proper diet" starting here>
http://www.karlloren.com/Diabetes/raw-food-diet.htm
This article was written when I realized that virtually ALL diabetes can be cured with proper diet -- and that the diet recommended by the American Diabetes Foundation is exactly the diet that will cause diabetes -- not unusual.
The lipomed is similar to the VAP, but uses NMR technology to classify particle size and number.
5. Out of curiosity, is your name pronounced LOR-en or Lo-REN?
My real name, driver's license, is Loren Carl Troescher. As a professional speaker, radio show host and author I use "Karl Loren." Both names are on my webs, here and there. "Loren" is pronounced "LOR en"
Troescher, in French, means either "very expensive" or "very sweet" depending on how it is pronounced. The name is German, would have an umlaut in it, and is pronounced differently by different parts of the family.
6. I agree with you about the failure of education. I have tried to instill in my students the idea that textbooks are written by people like their professors. They don't trust all of their professors, so why should they blindly trust their textbooks. Same thing for national guidelines. Unfortunately, most of the students simply want to be spoonfed.
Most people who criticize education blame the students. I blame those who teach teachers. If, by now, you have read my article on psychobabble you may realize the role of St. Thomas Aquinas, Dr. Wundt, Mr. Rockefeller, and John Dewey. I would come much closer to being willing to say the deliberate destruction of American Education was a conspiracy, but don't because the people who did it seem to have truly, but mistakenly, believed they were doing the right thing.
Drugs are another part of the problem, but the destruction of public schools started long before the drug epidemic. My method of "teaching" will seem revolutionary to you, I suspect, but it is being adapted in hundreds of places, quietly, but not in an electronic format -- which I am doing.
I really didn't see much disagreement here???
Karl
Second of many,
The term intravenous is used indiscriminately, but as you inferred should only truly be used to denote vein. A more general term would be intravascular. Based on the protocol you sent me regarding arteriograms, I can understand why there would be confusion. That procedure is a generalized procedure which could be used to visualize any artery in the body. In order to visualize the coronary arteries, you have to go in from an artery. If you go in from a vein, you'll end up in the right atrium. Generally coronary angiograms are done in a special room called a cath lab. The artery of choice is the right femoral. Sometimes, a brachial artery is chosen. The first thing done is the radiopaque die is injected into the left veintricle to assess ejection fraction and ventricular wall function. Then they try and get the catheter into each of the coronary arteries and inject the die there.
I find that definitions are vital in any communication -- all the more when a professor speaks to a guy that got by with only an MBA from Harvard.
Endothelial: A thin layer of flat epithelial cells that lines serous cavities, lymph vessels, and blood vessels.
Lesion: (1) A wound or injury. (2) A localized pathological change in a bodily organ or tissue. (3) An infected or diseased patch of skin.
I did not try to understand all the words in the definition of "endothelial" but I do see one striking word! I see the word "cells" in the plural. Immediately I know that either we are just not communicating, or we disagree on some part of this. I understand a blood vessel to include an "artery." I understand that the artery has three layers of "stuff" including a middle layer which is a muscle, and then an inner and an outer layer. Within these layers are individual "cells."
Near the bottom you do refer to "endothelial cells" rather than the "layer" made up of such cells -- but you can see how picky I am about definitions.
It is vital to understanding my concept of "plaque" to understand that I see the "plaque" (which I'll define below) as being INSIDE a living cell -- not anywhere else.
The usual explanation of plaque is that is a "layer" that coats the epithelial layer of cells.
From my web site, the below is the "usual" explanation of "plaque" as a layer of stuff, not inside individual cells, but "coating" the "inner lining" of an artery:
The inner lining of the normal coronary artery is smooth and free of
blockages or obstructions.
However, as we get older,
lipids or fatty substances (cholesterol and triglycerides) are deposited as
fatty streaks. The streaks are only minimally raised and thus do not produce
any obstruction or symptoms.
Patients with one or more risk factors for coronary artery disease are
susceptible to the increased buildup of fatty layers, known as atheroma
(pronounced athe-a-roma). This buildup of material begins to encroach
upon the inner channel and starts to interfere with the free flow of blood
through the coronary artery.
I call this description false! It is this false description which allows Lipitor to sell $10 billion of fraudulent drugs every year, and every medical doctor complicit in this crime. I speak harshly, but you seem to be willing to put up with that?
"Lesion" infers damage, probably of some sort of intrusion. My main point is made with the true description of WHERE plaque is, but there is this additional point of HOW this plaque got there. I would say, more accurately, that the individual cells in the muscle layer each contain several "calcium pumps" whose function is to regulate the amount of calcium INSIDE the cell (and control muscular contraction). These pumps are small enough that it is logical to think of a free radical as causing damage to a pump -- and many such free radicals can and do damage that pump so much that the pump no longer works properly, even though the cell is still "alive." The cell is hugely expandable, absorbs excessive calcium, creates extra cholesterol to thicken the membrane (as cells do) and THIS is the plaque. It is located and created very differently than any "endothelial lesion" that has ever been described.
Your professorial instruction on the angiogram is quite well appreciated here. I appreciate the technical language. But, out of your pleasant and lengthy letter, there is only this one line that is so fascinating:
Finally, regarding your hypothesis of "plaques"--I'll call them endothelial lesions--"real scientists" have known for years that the diet-cholesterol hypothesis was just plain wrong.
I've now commented on the "plaque" part of that sentence. I would have to re-read your earlier message about cholesterol, but even though you now call the "diet-cholesterol" hypothesis "plain wrong" I see billions of advertising dollars still be spent to promote harmful margarine, or scare people away from butter and eggs.
I have not yet seen you disagree, if you do, with my bolder assertion that "high cholesterol is NOT a risk factor for heart disease."
Is that worth pursuing?
I remember my cardiovascular physiology professor derogatorily referring to it as the hamburger hypothesis. The main difference between your theory and current true scientific theory, is your theory explains why the endothelium stops functioning in the first place.
It is interesting to see you contrasting "my theory" with "current true scientific theory." The truth is that the current truth is false and my theory accords with true science. Once you accept that free radicals are the base cause, you then look for what causes free radical (proliferation) and pretty soon you would be selling my oral chelation, and booted out of your job!
Unless you are using a different definition for "endothelium" than I found in the dictionary, I do not, anywhere, MY claim that this "layer" of stuff "stops functioning." I don't even claim that either the cells or the calcium pumps are irretrievably damaged -- only that they are damaged by free radicals, etc., as above.
The second area of divergence is the complete absence of lipoprotein in the theory. You're right that gross autopsy should not be able to detect whether the lesion is inside the endothelial cells or outside. But a patholgy or histological exam should be able to differentiate.
Lipoprotein was invented, my view, when the cholesterol lies needed to be covered up. One easy way to cover up lies is to introduce new confusing data, which can itself be false, but will serve the purpose for a while, until the yet-newer term of "good and bad" cholesterol can be invented.
One of the most fundamental flaws in most medical thinking is to confuse cause with effect -0- it is philosophical. Researchers see people with "high cholesterol" having heart problems, so conclude that the cholesterol causes the heart disease. Has it really been looked at how high cholesterol could be a symptom rather than a cause -- and a symptom of something that might well cause both high cholesterol AND heart disease -- not yet exposed because no drug will help? I could go on, but probably this has been enough for now?
I don't have sufficient data about either the existence or honesty of histological exams of calcium packed cells to comment. Do you?
Karl
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